Autophagy and toll-like receptors: a new link in cancer cells.
In addition to its clean-up function, autophagy is considered as an innate immunity mechanism due to its role in the removal of intracellular pathogens. Toll-like receptors (TLRs) are crucial components of innate immunity involved in the recognition of a diverse array of microbial products. Recent works demonstrated that different pathogen-associated molecular patterns (PAMPs) such as lipopolysaccharide (LPS) and single-strand RNA are able to induce autophagy via different TLRs in immune cells. In a recent report, we showed that bacterial CpG motifs, another PAMP, can induce autophagy in rodent and human tumor cell lines and that this process is TLR9-dependent. In addition, an increase in the number of autophagosomes can also be observed in vivo after the intratumoral injection of CpG motifs. These results extend the link between TLRs and autophagy to non-immune tumor cells and may be relevant for cancer treatment and more generally for gene therapy approaches in TLR9-positive tissues. In this addendum, we discuss the potential mechanisms and the consequences of the CpG-induced autophagy in tumor cells.
Bertin
Samuel
S
INSERM, Unité 638, Nice, France.
Pierrefite-Carle
Valérie
V
D001343:Autophagy / Q000276:immunology*; D018899:CpG Islands / Q000276:immunology*; D006801:Humans; D008024:Ligands; D008070:Lipopolysaccharides / Q000276:immunology; D009369:Neoplasms / Q000276:immunology* / Q000473:pathology; D009838:Oligodeoxyribonucleotides / Q000276:immunology / Q000494:pharmacology; D051193:Toll-Like Receptors / Q000819:agonists / Q000276:immunology*
C408982:CPG-oligonucleotide; D008024:Ligands; D008070:Lipopolysaccharides; D009838:Oligodeoxyribonucleotides; D051193:Toll-Like Receptors